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  • 1
    Online Resource
    Online Resource
    Homeostatic Regulation of Blood Neutrophil Counts
    The American Association of Immunologists ; 2008
    In:  The Journal of Immunology Vol. 181, No. 8 ( 2008-10-15), p. 5183-5188
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 181, No. 8 ( 2008-10-15), p. 5183-5188
    Abstract: Blood neutrophil counts are determined by the differentiation and proliferation of precursor cells, the release of mature neutrophils from the bone marrow, margination, trafficking and transmigration through the endothelial lining, neutrophil apoptosis, and uptake by phagocytes. This brief review summarizes the regulation of blood neutrophil counts, which is in part controlled by G-CSF, IL-17, and IL-23. Neutrophils are retained in the bone marrow through interaction of CXCL12 with its receptor CXCR4. The relevance of this mechanism is illustrated by rare diseases in which disrupting the desensitization of CXCR4 results in failure to release mature neutrophils from bone marrow. Although blood neutrophil numbers in inbred mouse strains and individual human subjects are tightly controlled, their large variation among outbred populations suggests genetic factors. One example is benign ethnic neutropenia, which is found in some African Americans. Reduced and elevated neutrophil counts, even within the normal range, are associated with excess all-cause mortality.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.181.8.5183
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2008
    detail.hit.zdb_id: 1475085-5
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  • 2
    Online Resource
    Online Resource
    Renal dysfunction increases aortic macrophage and lymphocyte accumulation during atherosclerosis development (102.2)
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 1_Supplement ( 2011-04-01), p. 102.2-102.2
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 1_Supplement ( 2011-04-01), p. 102.2-102.2
    Abstract: Atherosclerosis is a chronic inflammatory disease of the artery wall with innate and adaptive immune components. Decreased renal function is a major risk factor for cardiovascular events and mortality. While altered hemodynamics and mineral metabolism have been investigated in detail, the atherosclerotic vascular leukocyte infiltrate in renal impairment has not been systematically explored. This study tested whether moderate renal impairment alters leukocyte composition in the aorta of atherosclerotic mice. Apolipoprotein E deficient (Apoe-/-) mice underwent nephrectomy or sham surgery and were maintained on high-fat diet for 12 weeks. Aortic leukocyte infiltration was determined by immunofluorescence staining and confocal microscopy and by flow cytometry of aortic single cell suspensions. Unilateral nephrectomy significantly increased serum creatinine levels as a measure of renal function but did not alter serum calcium and phosphorous levels. While total blood leukocyte counts were un-altered, the number of aortic leukocytes was significantly increased after nephrectomy. Specifically, aortic B cells and macrophages were increased. Proliferation of aortic macrophages was increased. Aortic en face and root atherosclerotic lesion size were significantly larger in mononephric mice. We conclude that mild renal failure is sufficient to alter inflammatory aortic leukocyte accumulation in atherosclerosis.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.186.Supp.102.2
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
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  • 3
    Online Resource
    Online Resource
    Improved Survival and Reduced Vascular Permeability by Eliminating or Blocking 12/15-Lipoxygenase in Mouse Models of Acute Lung Injury (ALI)
    The American Association of Immunologists ; 2009
    In:  The Journal of Immunology Vol. 183, No. 7 ( 2009-10-01), p. 4715-4722
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 183, No. 7 ( 2009-10-01), p. 4715-4722
    Abstract: Acute lung injury (ALI) is a prevalent disease associated with high mortality. 12/15-lipoxygenase (12/15-LO) is an enzyme producing 12-hydroxyeicosatetraenoic acid (HETE) and 15-HETE from arachidonic acid. To test whether 12/15-LO is involved in increasing vascular permeability in the lung, we investigated the role of 12/15-LO in murine models of LPS-induced pulmonary inflammation and clinically relevant acid-induced ALI. The vascular permeability increase upon LPS inhalation was abolished in Alox15−/− mice lacking 12/15-LO and in wild-type mice after pharmacological blockade of 12/15-LO. Alox15−/− mice also showed improved gas exchange, reduced permeability increase, and prolonged survival in the acid-induced ALI model. Bone marrow chimeras and reconstitution experiments revealed that 12-HETE produced by hematopoietic cells regulates vascular permeability through a CXCR2-dependent mechanism. Our findings suggest that 12/15-LO-derived 12-HETE is a key mediator of vascular permeability in acute lung injury.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.0802592
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2009
    detail.hit.zdb_id: 1475085-5
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  • 4
    Online Resource
    Online Resource
    Defective Regulation of CXCR2 Facilitates Neutrophil Release from Bone Marrow Causing Spontaneous Inflammation in Severely NF-κB–Deficient Mice
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 185, No. 1 ( 2010-07-01), p. 670-678
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 185, No. 1 ( 2010-07-01), p. 670-678
    Abstract: NF-κB is a major regulator of innate and adaptive immunity. Neutrophilic granulocytes (neutrophils) constitutively express RelA/p65 (Rela), c-Rel (Crel), and p50 (Nfκb1) but not p52 (Nfκb2) subunits. In this paper, we describe Crel−/−Nfκb1−/−Rela+/− mice that have the most severe genetic neutrophil NF-κB deficiency compatible with life, Rela−/− mice being embryonic lethal. Crel−/−Nfκb1−/−Rela+/− mice developed spontaneous dermal and intestinal inflammation associated with chronic neutrophilia, elevated CXCL1, and G-CSF. The bone marrow contained fewer nucleated cells and was enriched in myeloid progenitor cells. Neutrophilia was preserved when Crel−/−Nfκb1−/−Rela+/− bone marrow was transferred into wild-type mice, but mixed bone marrow chimeras receiving wild-type and Crel−/−Nfκb1−/−Rela+/− bone marrow showed normal circulating neutrophil numbers, excluding an intrinsic proliferation advantage. In mixed bone marrow chimeras, Crel−/−Nfκb1−/−Rela+/− neutrophils were preferentially mobilized from the bone marrow in response to CXCL1 injection, LPS-induced lung inflammation, and thioglycollate-induced peritonitis. Crel−/−Nfκb1−/−Rela+/− neutrophils expressed higher levels of the CXCL1 receptor CXCR2 both under resting and stimulated conditions and failed to downregulate CXCR2 during inflammation. Treatment with an anti-CXCR2 Ab abolished preferential mobilization of Crel−/−Nfκb1−/−Rela+/− neutrophils in peritonitis in mixed chimeric mice and neutrophilia in Crel−/−Nfκb1−/−Rela+/− mice. We conclude that severe NF-κB deficiency facilitates neutrophil mobilization, which causes elevated numbers of preactivated neutrophils in blood and tissues, leading to spontaneous inflammation. These neutrophil effects may limit the usefulness of global NF-κB inhibitors for the treatment of inflammatory diseases.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1000339
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2010
    detail.hit.zdb_id: 1475085-5
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  • 5
    Online Resource
    Online Resource
    Inhibition of T cell proliferation decreases atherosclerotic lesion size revealing a role of IL-17 in mediating aortic CD11b+CD11c+ cell accumulation (35.4)
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 184, No. 1_Supplement ( 2010-04-01), p. 35.4-35.4
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 1_Supplement ( 2010-04-01), p. 35.4-35.4
    Abstract: Atherosclerosis is a chronic inflammatory disease of the artery wall with innate and adaptive immune components, however, immunosuppressive therapy is not uniformely beneficial. Mycophenolate suppresses lymphocyte proliferation by inhibiting inosine-monophosphate dehydrogenase. In this study, we tested whether mycophenolate inhibited atherosclerosis in apolipoprotein-E-deficient (Apoe-/-) mice. Apoe-/- mice treated with 30 mg/kg/day mycophenolate during 12 weeks of high fat diet showed significantly decreased aortic leukocyte infiltration. Flow cytometry at 3 and 12 weeks of high fat diet revealed significantly reduced aortic αβTCR+ cell content and reduced αβTCR+ cell proliferation as measured by BrdU incorporation. Aortic atherosclerotic lesion sizes were significantly reduced. Among T cell cytokines, IL-17 was significantly reduced in plasma of mycophenolate-treated mice. IL-17 receptor A was expressed on both blood monocytes and aortic CD11b+CD11c+ cells. Proliferation and aortic content of CD11b+CD11c+ cells and plasma levels of IL-6 and TNF-α were reduced. CD11b+CD11c+ cells in aortas of IL-17 receptor deficient mice after 12 weeks of high fat diet were significantly reduced compared to wild-type mice. Our data suggest that that mycophenolate curbs IL-17 production, which in turn limits myeloid cell accumulation in atherosclerosis. Since mycophenolate is approved for human use, this suggests its potential application for prevention and/or therapy.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.184.Supp.35.4
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2010
    detail.hit.zdb_id: 1475085-5
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  • 6
    Online Resource
    Online Resource
    Dynamic T cell–APC interactions sustain chronic inflammation in atherosclerosis
    American Society for Clinical Investigation ; 2012
    In:  Journal of Clinical Investigation Vol. 122, No. 9 ( 2012-9-4), p. 3114-3126
    Details
    In: Journal of Clinical Investigation, American Society for Clinical Investigation, Vol. 122, No. 9 ( 2012-9-4), p. 3114-3126
    Type of Medium: Online Resource
    ISSN: 0021-9738
    URL: Article
    URL: Article
    DOI: 10.1172/JCI61758
    DOI: 10.1172/JCI61758DS1
    Language: English
    Publisher: American Society for Clinical Investigation
    Publication Date: 2012
    detail.hit.zdb_id: 2018375-6
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  • 7
    Online Resource
    Online Resource
    Interleukin 17A controls Interleukin 17F production to maintain precise regulation of blood neutrophil counts in mice (133.8)
    The American Association of Immunologists ; 2009
    In:  The Journal of Immunology Vol. 182, No. 1_Supplement ( 2009-04-01), p. 133.8-133.8
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 182, No. 1_Supplement ( 2009-04-01), p. 133.8-133.8
    Abstract: Granulocyte colony-stimulating factor (G-CSF), its receptor and interleukin-17 receptor A (IL-17RA) are all required to maintain baseline neutrophil counts in mice. Here, we tested whether IL-17F could compensate and maintain baseline neutrophil counts in the absence of IL-17A. Unlike the reduced neutrophil counts found in IL-17RA deficient mice, neutrophil counts were mildly increased in IL-17A deficient (Il17a-/-) animals. There was no evidence for infection or altered neutrophil function. Plasma G-CSF and IL-17F levels were elevated in Il17a-/- compared to wild-type mice. IL-17F was mainly produced in the spleen and mesenteric lymph nodes, but IL-23 was unaltered in Il17a-/- mice. Instead, Il17a-/- splenocytes differentiated with IL-6, TGF-β and IL-23 ex-vivo produced significantly more IL-17F in response to IL-23 than wild-type cells. Adding recombinant IL-17A to Il17a-/-splenocyte cultures reduced IL-17F mRNA and protein secretion. These effects were also observed in wild-type but not IL-17RA deficient cells. We conclude that IL-17A mediated suppression of IL-17F production and secretion is relevant to maintain the normal setpoint of blood neutrophil counts in vivo.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.182.Supp.133.8
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2009
    detail.hit.zdb_id: 1475085-5
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  • 8
    Online Resource
    Online Resource
    Interleukin 17 in vascular inflammation
    Elsevier BV ; 2010
    In:  Cytokine & Growth Factor Reviews Vol. 21, No. 6 ( 2010-12), p. 463-469
    Details
    In: Cytokine & Growth Factor Reviews, Elsevier BV, Vol. 21, No. 6 ( 2010-12), p. 463-469
    Type of Medium: Online Resource
    ISSN: 1359-6101
    URL: Article
    DOI: 10.1016/j.cytogfr.2010.10.003
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2010
    detail.hit.zdb_id: 2025966-9
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  • 9
    Online Resource
    Online Resource
    Mycophenolate Mofetil Decreases Atherosclerotic Lesion Size by Depression of Aortic T-Lymphocyte and Interleukin-17–Mediated Macrophage Accumulation
    Elsevier BV ; 2011
    In:  Journal of the American College of Cardiology Vol. 57, No. 21 ( 2011-05), p. 2194-2204
    Details
    In: Journal of the American College of Cardiology, Elsevier BV, Vol. 57, No. 21 ( 2011-05), p. 2194-2204
    Type of Medium: Online Resource
    ISSN: 0735-1097
    URL: Article
    DOI: 10.1016/j.jacc.2010.12.030
    RVK:
    XA 17760
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2011
    detail.hit.zdb_id: 1468327-1
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  • 10
    Online Resource
    Online Resource
    Mycophenolic acid suppresses granulopoiesis by inhibition of interleukin-17 production
    Elsevier BV ; 2010
    In:  Kidney International Vol. 78, No. 1 ( 2010-07), p. 79-88
    Details
    In: Kidney International, Elsevier BV, Vol. 78, No. 1 ( 2010-07), p. 79-88
    Type of Medium: Online Resource
    ISSN: 0085-2538
    URL: Article
    DOI: 10.1038/ki.2010.84
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2010
    detail.hit.zdb_id: 2007940-0
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